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PHYSIOLOGY OF HOST-PARASITE INTERACTION

1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM

2. HISTOPATHOLOGICAL AND ULTRASTRUCTURAL OF PATHOGENESIS

3. BIOCHEMICAL OF PATHOGENESIS:

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ENZYME AND TOXIN OF COCHLIOBOLUS

INFECTION

Trophic system:

1. Mutualistic Symbiont

2. Biotroph3. Hemibiotroph

4. Necrotroph

5. Saprotroph

Degree of specialization:

High

Low

More physiological synchronization between host-pathogen

- Cause minimum effect to their host and inceasedependence to living host cell

- Less dependence to wall degrading enzyme and toxin- Selective and site specific use of enzyme- Selective of involvement of phytohormone- Restricted host range- Synchronize physiological process of host-pathogen

- Cause extensive damage to the host by degradingenzyme > secondary toxic metabolites

- More dependence to the host- Less saprophytic ability

1.FUNGAL CLASSIFICATION :TROPHIC SYSTEM

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1. HISTOPATOLOGICAL AND ULTRASTUCTURAL OF PATHOGENESIS

Cladosporium fulvum:

- Caused leaf spot (necrotic) of tomato- Attach to the leaf by extracellular protein (EP)

- Infection on lower surface of the leave, plant response towards avirulent andvirulent strain, differ

- Conidia germinate to form runner hyphae (2-3 um) until open stomata found,penetrate (3-5 days after inoculation), hyphae enlarge (4-5um), grow intercellularly

- penetration peg

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HR

- Hyphae in close contact to mesophyll, do not form haustoria and no defenseresponse on succeptible cultivar

- After penetration, fungal growth arrested, hypersensitive (HR) defense reaction onresistant cultivar , mesophyll cells accumulates substance

- Within 2 weeks conidia were formed on the lesion on succeptible, but not onresistant cultivar

basic compatibilty

specific-racecompatibility

COMPATIBILITY

produce glycoprotein,non specific elicitor

• Induce necrosis in tomato leaves• Not race specific

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Produce and accumulate phytoalexinElectrolyte leakageIncrease lipoxygenaseIncrease lipoperoksidase

2. BIOCHEMICAL OF INTERACTION

A. Extracellular substanse, non specific elicitorCladosporium fulvum

Hypesensitive reaction

• Helminthosporoside Cohliobolus sacchari, pathogen of sugarcane

1 of 3 isomer of sesquiterpenoids binds to 1-4 galactofuranose by linkage

- if contain less than 4 galactose unit inactive or protect sugarcane against HS-toxin- B. Sacchari, anamorph, produce galactofuranosidase that remove galactose from HS-

toxin

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• HV-toxin (Victorin) C. victoriae on oat var. victoria----- blight• T-toxin• HC-toxin

C. heterosporus race T on maize Texas male sterile cytoplasm (Tcms)C. carbonum race 1 on maize (inbread line) ------ blight

Do not play a major role in host-parasite interaction

B. ENZYME AND TOXINCOCHLIOBOLUS

1. Enzyme:- CWDEs:

a. endoplygalacturonase and endo-xylanase, toxic and induce phytoalexin accumulationb. Cellulose, pectinase, endo=polygalacturonase degrading enzyme

2. HS (Host selective)- Toxin:

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C. INFECTION

a. PENETRATION OF CUTICLE

b. ENTRY THROUGH CELL WALL

c. PLANT DEFENCE: - DETOXIFICATION OF PHYTOALEXIN

- PRODUCTION OF ANTI-FUNGAL PROTEIN

a. CUTICULAR PENETRATION

Penetration by:Physical force with assistance of degrading enzyme

Enzymatic degradation:Germinating spore (tips of germ tube) F. Solani f.sp pisi produce

cutinase: depolymerize cutin

Diisopropylfluorophosphate (DFP)N-butylisocyanate (benomyl)Organophosphoric fungiside ( serine inhibitors, 6-chloro-2-pyrone

derivates)

cuticle rupture

cutinase inhibitor,prevent cuticle rupture

no infection

Cutinase: inducible enzyme• Ability to degrade cutin (production of cutinase) ----------- degree of virulence• Rupture cuticle -------------------- not induce cutinase production• Avirulent isolate ----------low cutinase producer-------penetrate through stomata or wound

Cutinase gene expression:• Virulence isolate : multicopy of cutinase gene• Avirulent isolate : single copy of cutinase gene• Spores of highly virulent strain have cutinase but not sufficient for infection,

for cutin surface recognition

• Contact with cutin-------------- induce cutinase production synthesis• Transcription ------------------- 15 min after contact with cutin

• Cutin monomers (hydroxy acids) ----------- true inducers ----------- plant suceptibility

Transcription:Cutinase gene ------ 135 bp, four promoter and a silencer, a positive acting G-rich element

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b. Entry

Fungi

through cell wall

produce endo and exopectinase, and endopectate lyase

degrade

Pectin: major cell wall component

Self catabolite repression

demetylate

Less inhibitory product

- Detoxification of phytoalexin

Pea phytoalexin:- pisatin (isoflavonoid compound)- absent in healthy plant- accumulate, 5% dry weight, a few days after infection F. solani fsp. pisi

(N. Haematococca)

P40 cytochrome demethylasePisatininduce

repress

glucose

VirulenceHigh, tolerate , demethylate pisatinLow, sensitive , could not demetylate pisatin

Gene control pisatin production: P da gene, meiotic instable

May be lost

c. Plant defence

1. Reinforcing cell wall to limit ingress of pathogens: production ofphenolic substance

2. Producing antifungal protein3. Producing phytoalexin:

- a low molecular weight toxic compound to fungi- synthesize and accumulate at the site of infection after exposure to

pathogen

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- Production of anti-fungal protein

Plant pathogen or pathogen elicitors

Altered protein synthesis , including anti-fungal protein2 chitinase and 2 1,3 glucanase

Degrade or inhibit fungal pathogen degrade chitin degrade glucan

Fungal cell wall

Glycosidic fragment

Chitosan, hexosamine fragment

Pisatin production in plant Inhibits fungal growth

3. MATING TYPE AND PATHOGENESISINFECTION

• Important for smut as fusion ofhaploid cells of opposite matingtype is prerequisite for infection

• Dikaryotic hyphae developed inhost tissue

• Promycelium may infect hostdirectly

• Mat locus of U. maydis (a1 and a2formed pheromone andpheromone receptors)

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